Stimulatory device and methods to electrically stimulate the phrenic nerve

ABSTRACT

The invention provides exemplary devices and methods electrically stimulating the phrenic nerve. In one embodiment, electrodes are placed posterior and anterior in the region of the cervical vertebrae. Electrical current having a multi-phasic waveform is periodically applied to the electrodes to stimulate the phrenic nerve, thereby causing the diaphragm to contract.

CROSS-REFERENCES TO RELATED APPLICATIONS

[0001] This application is a continuation in part application of U.S.patent application Ser. No. 09/315,396, filed May 20, 1999, which is acontinuation in part application of U.S. patent application Ser. No.09/197,286, filed Nov. 20, 1998, which is a continuation in partapplication of U.S. patent application Ser. No. 09/095,916, filed Jun.11, 1998, the complete disclosures of which are herein incorporated byreference.

BACKGROUND OF THE INVENTION

[0002] The invention relates generally to the field of cardiopulmonaryresuscitation, artificial ventilation, treatment of various types ofshock, and treatment of right ventricular failure. In particular, thepresent invention in some embodiments relates to devices and methods forincreasing blood flow to the thorax, including increasingcardiopulmonary circulation during cardiopulmonary resuscitationprocedures. In one aspect, increased blood flow to the thorax isaccomplished by electrically stimulating the phrenic nerve. Stimulationof the phrenic nerve may also be used to ventilate a patient.

[0003] Worldwide, sudden cardiac arrest is a major cause of death and isthe result of a variety of circumstances, including heart disease andsignificant trauma. In the event of a cardiac arrest, several measureshave been deemed to be essential in order to improve a patient's chanceof survival. These measures must be taken as soon as possible to atleast partially restore the patient's respiration and blood circulation.One common technique, developed approximately 30 years ago, is anexternal chest compression technique generally referred to ascardiopulmonary resuscitation (CPR). CPR techniques have remainedlargely unchanged over the past two decades. With traditional CPR,pressure is applied to a patient's chest to increase intrathoracicpressure. An increase in intrathoracic pressure induces blood movementfrom the region of the heart and lungs towards the peripheral arteries.Such pressure partially restores the patient's circulation.

[0004] Traditional CPR is performed by active compression of the chestby direct application of an external pressure to the chest. This phaseof CPR is typically referred to as the compression phase. After activecompression, the chest is allowed to expand by its natural elasticitywhich causes expansion of the patient's chest wall. This phase is oftenreferred to as the relaxation or decompression phase. Such expansion ofthe chest allows some blood to enter the cardiac chambers of the heart.The procedure as described, however, is insufficient to ventilate thepatient. Consequently, conventional CPR also requires periodicventilation of the patient. This is commonly accomplished by amouth-to-mouth technique or by using positive pressure devices, such asa self-inflating bag which delivers air through a mask, an endotrachealtube, or other artificial airway.

[0005] In order to increase cardiopulmonary circulation induced by chestcompression, a technique referred to as active compression-decompression(ACD) has been developed. According to ACD techniques, the activecompression phase of traditional CPR is enhanced by pressing anapplicator body against the patient's chest to compress the chest. Suchan applicator body is able to distribute an applied force substantiallyevenly over a portion of the patient's chest. More importantly, however,the applicator body is sealed against the patient's chest so that it maybe lifted to actively expand the patient's chest during the relaxationor decompression phase. The resultant negative intrathoracic pressureinduces venous blood to flow into the heart and lungs from theperipheral venous vasculature of the patient. Devices and methods forperforming ACD to the patient are described in U.S. Pat. Nos. 5,454,779and 5,645,552, the complete disclosures of which are herein incorporatedby reference.

[0006] Another successful technique for increasing cardiopulmonarycirculation is by impeding air flow into a patient's lungs during therelaxation or decompression phase. By impeding the air flow during therelaxation or decompression phase, the magnitude and duration ofnegative intrathoracic pressure is increased. In this way, the amount ofblood flow into the heart and lungs is increased. This creates a vacuumin the chest. As a result, cardiopulmonary circulation is increased.Devices and methods for impeding or occluding the patient's airwayduring the relaxation or decompression phase are described in U.S. Pat.Nos. 5,551,420 and 5,692,498 and co-pending U.S. application Ser. No.08/950,702, filed Oct. 15, 1997. The complete disclosures of all thesereferences are herein incorporated by reference.

[0007] The above techniques have proven to be extremely useful inenhancing traditional CPR procedures. As such, it would be desirable toprovide still further techniques to enhance venous blood flow into theheart and lungs of a patient from the peripheral venous vasculatureduring both conventional and alternative CPR techniques. It would beparticularly desirable to provide techniques which would enhanceoxygenation and increase the total blood return to the chest during therelaxation or decompression phase of CPR.

[0008] In additional to CPR techniques, other situations exist whereblood flow to the thorax is important. Hence, the invention is alsorelated to techniques for returning blood to the thorax for otherreasons, i.e., for treating various types of shock, right ventricularfailure, post resuscitation pulseless electrical activity, and the like.The invention is also related to providing novel techniques to ventilatea patient, especially in cases where intubation is undesirable or whereventilation can result in the bursting of pulmonary alveoli andbronchioles.

SUMMARY OF THE INVENTION

[0009] In certain embodiments, the invention provides methods anddevices for increasing cardiopulmonary circulation when performingcardiopulmonary resuscitation. The methods and devices may be used inconnection with most generally accepted CPR methods. In one exemplarymethod, a patient's chest is actively compressed during the compressionphase of CPR. At least some of the respiratory muscles, and particularlythe inspiratory muscles, are then stimulated to contract during therelaxation or decompression phase to increase the magnitude and prolongthe duration of negative intrathoracic pressure during the relaxation ordecompression phase, i.e., respiratory muscle stimulation increases theduration and degree that the intrathoracic pressure is below or negativewith respect to the pressure in the peripheral venous vasculature. Byenhancing the amount of venous blood flow to the heart and lungs,cardiopulmonary circulation is increased.

[0010] Among the respiratory muscles that may be stimulated to contractare the diaphragm and the chest wall muscles, including the intercostalmuscles. The respiratory muscles may be stimulated to contract in avariety of ways. For example, the diaphragm may be stimulated tocontract by supplying electrical current or a magnetic field to variousnerves or muscle bundles which when stimulated cause the diaphragm tocontract. Similar techniques may be used to stimulate the chest wallmuscles to contract. A variety of pulse trains, pulse widths, pulsefrequencies and pulse waveforms may be used for stimulation. Further,the electrode location and timing of pulse delivery may be varied. Inone particular aspect, an electrical current gradient or a magneticfield is provided to directly or indirectly stimulate the phrenic nerve.

[0011] To electrically stimulate the inspiratory motor nerves,electrodes are preferably placed on the lateral surface of the neck overthe point where the phrenic nerve, on the chest surface just lateral tothe lower sternum to deliver current to the phrenic nerves just as theyenter the diaphragm, on the upper chest just anterior to the axillae tostimulate the thoracic nerves, in the oral pharyngeal region of thethroat, or on the larynx itself. However, it will be appreciated thatother electrode sites may be employed. For example, in one embodimentthe respiratory muscles are stimulated by a transcutaneous electricalimpulse delivered along the lower antero-lat margin of the rib cage. Inone embodiment, inspiration is induced by stimulating inspiratorymuscles using one or more electrodes attached to an endotracheal tube orpharyngeal tube.

[0012] A variety of other techniques may be applied to further enhancethe amount of venous blood flow into the heart and lungs during thechest relaxation or decompression phase of CPR. For example, the chestmay be actively lifted during the relaxation or decompression phase toincrease the amount and extent of negative intrathoracic pressure.Alternatively, the chest may be compressed by a circumferential binder.Upon release, the chest recoil enhances venous return. During interposedcounterpulsation CPR, pressing on the abdomen in an alternating fashionwith chest compression also enhances blood return to the heart. Inanother technique, air flow to the lungs may be periodically occludedduring at least a portion of the relaxation or decompression phase. Suchocclusion may be accomplished by placing an impedance valve into thepatient's airway, with the impedance valve being set to open afterexperiencing a predetermined threshold negative intrathoracic pressure.

[0013] In one particular aspect of the method, respiratory gases areperiodically supplied to the patient's lungs to ventilate the patient.In another aspect, a metronome is provided to assist the rescuer inperforming regular chest compressions.

[0014] In still another aspect, the respiratory muscles are stimulatedonly during certain relaxation or decompression phases, such as everysecond or third relaxation or decompression phase. In yet anotheraspect, a defibrillation shock is periodically delivered to the patientto shock the heart or an electrical impulse is delivered to periodicallyinitiate transthoracic pacing.

[0015] The invention further provides an exemplary device to assist inthe performance of a cardiopulmonary resuscitation procedure. The devicecomprises a compression member which is preferably placed over thesternum and manually or mechanically pressed to compress the chest. Atleast one electrode is coupled to the compression member in a way suchthat the electrode will be positioned to supply electrical stimulationto the respiratory muscles to cause the respiratory muscles to contractfollowing compression of the chest.

[0016] In one preferable aspect, a pair of arms extend from thecompression member, with one or more electrodes being coupled to the endof each arm. Preferably, the arms are fashioned so as to be adapted tobe received over the lower rib cage when the compression member is overthe sternum. In this way, the electrodes are placed in a preferredlocation to stimulate the respiratory muscles to contract. Conveniently,the arms may be fashioned of a flexible fabric so that the arms willconform to the shape of the chest, thereby facilitating proper placementof the electrodes. In one preferable aspect, the electrodes compriseadhesive electrically active pads.

[0017] In one particular aspect, a voltage controller or a potentiometeris provided to control the stimulation voltage delivered to theelectrode. In this way, a rescuer or a closed loop feedback system maychange the voltage output of the electrode to ensure adequaterespiratory muscle stimulation. A metronome may optionally be providedand incorporated into the device to assist a rescuer in performingregular chest compressions with the compression member. In anotheraspect, the stimulation sites may be varied on a periodic basis with anautomatic switching box to avoid respiratory muscle or chest wall musclefatigue.

[0018] In one particularly preferable aspect, a pressure or force sensoris disposed in the compression member to sense when a compressive forceis being applied to the compression member. Control circuitry may alsoprovided to cause actuation of the electrode when the sensor senses anexternal compression that is being applied to the compressive member. Inthis way, a sensor-directed electrical impulse may be emitted from theelectrode to transcutaneously stimulate the respiratory muscles tocontract at the end of the compression phase. Endotracheal stimulationof respiration muscles is also possible in a similar manner. In caseswhere a significant delay occurs between delivery of the stimulant andfull respiratory muscle contraction, the sensor may be employed to sensewhen mid-compression (or some other point in the compression phase)occurs to initiate respiratory muscle stimulation sometime before thestart of the relaxation or decompression phase.

[0019] In still another aspect, a power source is coupled to theelectrode. The power source may be integrally formed within the deviceor may be a separate power source which is coupled to the electrode. Asanother alternative, the electrode may be coupled to a defibrillator toprovide a defibrillation shock or to initiate trans-thoracic cardiacpacing. In another aspect, the voltage controller and power source maybe part of a sensor-compression-stimulation device or coupled to thedevice but separated from the compression-sensor-stimulation device. Instill another alternative, the device may be coupled to a ventilator toperiodically ventilate the patient based on the number of compressions.In another aspect, impedance or electrical impulses generated by chestcompression may be sensed and used by a remote power source andpacer-defibrillation unit to stimulate respiratory muscle contractionusing the same sensing electrode(s) or other means to also stimulate therespiratory muscles to contract.

[0020] The invention further provides an exemplary device to assist inthe performance of cardiopulmonary resuscitation by stimulating thephrenic nerve to cause the diaphragm and/or other respiratory muscles tocontract during the relaxation or decompression phase of CPR. Suchstimulation may be accomplished by delivering either electrical ormagnetic energy to the phrenic nerve. In one embodiment, the phrenicnerve stimulators may be coupled to a chest compression sensor tocoordinate chest compressions with the electric or magnetic stimulationof the phrenic nerve. In another aspect, a signal, such as an audiblesignal or blinking light, may be produced each time electricalinspiration occurs, and manual chest compression is timed based on theemitted signal.

[0021] In another embodiment, the device comprises a ventilation memberwhich is coupled to the patient's airway to assist in the flow ofrespiratory gases into the patient's lungs. A sensor may be coupled tothe ventilation member to induce application of an electrical current tothe phrenic nerve to cause the diaphragm or other respiratory muscles tocontract. In this way, a ventilation member which is typically employedto provide ventilation to a patient during a CPR procedure may alsofunction as a stimulant to cause contraction of the diaphragm or otherrespiratory muscles during the relaxation or decompression phase of CPR.In this manner, the amount of venous blood flowing to the heart andlungs will be enhanced.

[0022] A variety of ventilation members may be employed, includingendotracheal tubes, laryngeal mask airways, or other ventilation deviceswhich are placed within the larynx, esophagus, or trachea. In oneparticularly preferable aspect, a pair of electrodes is coupled to theventilation member so that the device may operate in a unipolar ormultipolar manner to stimulate the phrenic nerve. Other aspects includetranscutaneous phrenic nerve stimulation with a collar-like deviceplaced around the neck which includes one or more electrodes located onboth anterior and posterior surfaces to stimulate the phrenic nerve.

[0023] In another embodiment, a system is provided to produce a cough.The system comprises at least one electrode that is adapted to bepositioned on a patient to stimulate the abdominal muscles to contract.A valve is also provided and has an open position and a closed position.A controller is coupled to the electrode and the valve and is configuredto open the valve after the electrode is actuated to cause the patientto cough,. i.e. the valve allows pressure to build, then opens torelease pressure and enhance expiratory gas flow rate similar to acough. In one aspect, the controller is configured to open the valve fora time in the range from about 10 ms to about 500 ms after the abdominalmuscles are stimulated to contract.

[0024] The invention further provides an exemplary method for increasingcardiopulmonary circulation when performing cardiopulmonaryresuscitation on a patient in cardiac arrest. According to the method,at least some of the abdominal muscles are periodically stimulated tocontract sufficient to enhance the amount of venous blood flow into theheart and lungs. In one aspect, the abdominal muscles may beelectrically stimulated to contract while preventing respiratory gasesfrom exiting the lungs, and then permitting respiratory gases fromexiting the lungs to produce a cough. In another aspect, the patient'schest is actively compressed during a compression phase and thepatient's chest is permitted to rise during a decompression phase.Further, the abdominal muscles are stimulated to contract during a timeperiod which ranges between a latter portion of the decompression phaseto a mid portion of the compression phase.

[0025] In another embodiment, a method is provided for increasing bloodflow to the thorax of a patient. According to the method, the phrenicnerve is periodically stimulated to cause the diaphragm to contract andthereby causing an increase in the magnitude and duration of negativeintrathoracic pressure. This results in a “gasp” creating a vacuum,thereby sucking more air and blood into the thorax. Further, whenairflow is periodically occluded from flowing to the lungs duringcontraction of the diaphragm with a valve that is positioned to controlairflow into the patient's airway, the magnitude and duration ofnegative intrathoracic pressure is further increased to force more bloodinto the thorax.

[0026] In one particular aspect, the phrenic nerve is stimulated byapplying electrical current to the phrenic nerve with electrodes thatare positioned over the cervical vertebrae between C3 and C7. Morepreferably, the electrodes are placed both posterior and anteriorbetween C3 and C5. In another aspect, the electrical current is providedin multiphasic form. For example, the wave form may be biphasic,including asymmetrical biphasic. Depending on the particular treatment,the electrical signal may be within certain current ranges, certainfrequency ranges, and certain pulse width ranges. Merely by way ofexample, biphasic electrical current may be used that is in the rangefrom about 100 milliamps to about 2,000 milliamps at a frequency in therange from about 10 Hz to about 100 Hz, and in pulse widths in the rangefrom about 1 μs to about 5 ms.

[0027] The methods of the invention may also be used to treat a widevariety of conditions, including for example, hemorrhagic shock,hypovolemic shock, cardiogenic shock, post resuscitation pulselesselectrical activity, right ventricular failure, and the like. Forinstance, when the patient is suffering from hemorrhagic shock, thephrenic nerve may be stimulated about 5 to about 30 times per minute.Further, the phrenic nerve may be stimulated after each breath for timeintervals of about 0.25 seconds to about 5 seconds, or in the range fromabout twice per every one breath to about once about every five breaths.For hypovolemic shock, the phrenic nerve may be stimulated about 5 toabout 40 times per minute. When suffering from cardiogenic shock, thephrenic nerve may be stimulated about 5 to about 80 times per minute.

[0028] In some cases, the patient may be suffering from cardiac arrest,and the phrenic nerve may be stimulated about 10 to about 100 times perminute in combination with chest compressions that are performed at arate in the range from about 50 compressions to about 100 compressionsper minute. In one option, the chest compressions may be sensed and usedto control the timing of phrenic nerve stimulations. Alternatively, arepeating audio and/or visual signal may be provided to indicate to arescuer when to perform the chest compressions based on the timing ofphrenic nerve stimulation. Such a process is described in greater detailin copending U.S. patent application Ser. No. _________, filed on thesame date as the present application (Attorney Docket No. 16354-004000),the complete disclosure of which is herein incorporated by reference. Inanother option, the number of chest compressions relative to the numberof phrenic nerve stimulations may be counted.

[0029] For patients suffering from post resuscitation pulselesselectrical activity, the phrenic nerve may be stimulated about 5 toabout 60 times per minute. When suffering from right ventricularfailure, the phrenic nerve may be stimulated about 5 to about 80 timesper minute. The duration of the stimulation may last from 0.25 to about6 seconds.

[0030] In another embodiment, a method is provided for ventilating apatient, such as when the patient is suffering from respiratory distressor apnea. According to the method, electrodes are placed posterior andanterior on the cervical vertebrae, such as in the C3 to C5 region.Electrical current having a multiphasic waveform, such as an asymmetricbiphasic waveform, is supplied to the electrodes to stimulate thephrenic nerve, thereby causing the diaphragm to contract and drawrespiratory gases into the patient's lungs. Conveniently, the phrenicnerve may be stimulated about 3 to about 30 times per minute.

[0031] In still another embodiment, a method is provided for increasingblood flow to the thorax of a patient by repeatedly electricallystimulating the diaphragm to contract with at least two electrodes. Themagnitude of negative intrathoracic pressure is sensed afterdiaphragmatic stimulation, and the amount of current that is supplied tothe electrode is controlled based on the measured pressure. For example,the sensed measurement may be used to continually adjust the currentlevel so that the magnitude of negative intrathoracic pressure is withinthe range from about −5 mmHg to about −30 mmHg during diaphragmaticstimulation.

[0032] In another embodiment, a stimulation device is provided thatcomprises a generally flat back plate that is configured to be placedbelow a patient's back when the patient is lying down. A neck support iscoupled to the back plate and serves to tilt the patient's headbackward. Further, at least two electrodes are coupled to thestimulation device to electrically stimulate the patient. For example,the electrodes may be employed to electrically stimulate the phrenicnerve in a manner similar to other embodiments described herein.Optionally, a pair of defibrillation electrodes may also be coupled tothe stimulation device to permit a defibrillating shock to be applied.

BRIEF DESCRIPTION OF THE DRAWINGS

[0033]FIG. 1 is a top plan view of an exemplary respiratory musclestimulation device according to the invention.

[0034]FIG. 2 is a side view of the device of FIG. 1.

[0035]FIG. 3 is a detailed bottom view of an end member of the device ofFIG. 1 showing an electrode for stimulating the respiratory muscles.

[0036]FIG. 4 illustrates a top view of the end member of FIG. 3 showinga potentiometer, a metronome, and a power source.

[0037]FIG. 5 is a top plan view of an alternative embodiment of arespiratory muscle stimulation device according to the invention.

[0038]FIG. 5A illustrates yet another alternative embodiment of arespiratory muscle stimulation device according to the invention.

[0039]FIG. 6 is a block diagram of the circuitry of the device of FIG. 1according to the invention.

[0040]FIG. 7 illustrates the device of FIG. 1 when used to treat apatient according to the invention.

[0041]FIG. 8 illustrates an exemplary endotracheal tube having a pair ofelectrodes to electrically stimulate the phrenic nerve according to theinvention.

[0042]FIG. 8A illustrates a collar to electrically or magneticallystimulate diaphragmatic stimulation according to the invention.

[0043]FIG. 8B illustrates the endotracheal tube of FIG. 8 having aplurality of electrodes disposed on an inflatable cuff according to theinvention.

[0044]FIG. 9 is a schematic diagram of an exemplary system forstimulating the respiratory muscles to contract while performing CPR.

[0045]FIG. 10 illustrates a blanket having electrodes for stimulatingthe respiratory muscles to contract according to the invention.

[0046]FIG. 11 schematically illustrates a system for stimulating theabdominal muscles according to the invention.

[0047]FIG. 12 illustrates a system for respiratory gas occlusion andabdominal stimulation according to the invention.

[0048]FIG. 12A illustrates a facial mask of the system of FIG. 12.

[0049]FIG. 12B illustrates an endotracheal/abdominal stimulation systemaccording to the invention.

[0050]FIG. 13 is a circuit block diagram of a system for electricallystimulating the diaphragm according to the invention.

[0051]FIG. 14 is a top view of a compression pad that may be used withthe system of FIG. 13.

[0052]FIG. 15 is a cross sectional side view of the compression pad ofFIG. 14.

[0053]FIG. 16 illustrates a circuit diagram of an input control switchof the system of FIG. 13.

[0054]FIG. 17 illustrates a circuit diagram of a manual switchcontroller of the system of FIG. 13.

[0055]FIG. 18 illustrates a circuit diagram of an input signal anddisplay module of the system of FIG. 13.

[0056]FIG. 19 illustrates a circuit diagram of a compressioncounter/reset module of the system of FIG. 13.

[0057]FIG. 20 illustrates a circuit diagram of a sense and displaymodule of the system of FIG. 13.

[0058]FIG. 21 illustrates a circuit diagram of a stimulator ON adjustmodule of the system of FIG. 13.

[0059]FIG. 22 is a flow chart illustrating methods for stimulatingdiaphragmatic compression in connection with chest compressions.

[0060]FIG. 23 is a schematic diagram of a transthoracic electrode mapshowing electrode placements for one example of the invention.

[0061]FIG. 24A is a schematic diagram of an electrode map showinganterior electrode positions for one example of the invention.

[0062]FIG. 24B is a schematic diagram of an electrode map showingposterior electrode positions for one example of the invention.

[0063]FIG. 25 is a graph illustrating the applied voltage to theelectrodes of FIGS. 24A and 24B and the resulting negative intrathoracicpressure when using an impedance valve.

[0064]FIG. 26 is a graph illustrating the applied voltage to theelectrodes of FIGS. 24A and 24B and the resulting negative intrathoracicpressure without the use of an impedance valve.

[0065]FIG. 27 is a graph illustrating the tidal volumes achieved at thecorresponding negative intrathoracic pressures of the graph of FIG. 26.

[0066]FIG. 28A is a schematic diagram of an alternative electrode mapshowing an anterior electrode position for one example of the invention.

[0067]FIG. 28B is a schematic diagram of an electrode map showing aposterior electrode positions for one example of the invention.

[0068]FIG. 29 is a schematic diagram of a stimulation device accordingto the invention.

[0069]FIG. 30 is a schematic view of an alternative stimulation deviceaccording to the invention.

[0070]FIG. 31 is a schematic top view of a stimulation collar systemthat is attached to a patient according to the invention.

[0071]FIG. 32 is a top view of the system of FIG. 31 when removed fromthe patient.

[0072]FIG. 33 is an end view of the system of FIG. 32.

[0073]FIG. 34 is a side view of another embodiment of a neck collarhaving stimulating electrodes according to the invention.

[0074]FIG. 35 is a top perspective view of a lifting device that may beused when treating a patient suffering from hypovolemic or hemorrhagicshock according to the invention.

[0075]FIG. 35 is a cross sectional side view of the device of FIG. 35.

DESCRIPTION OF THE SPECIFIC EMBODIMENTS

[0076] The present invention in certain embodiments provides methods anddevices for increasing cardiopulmonary circulation when performingcardiopulmonary resuscitation. As is known in the art, cardiopulmonaryresuscitation techniques involve a compression phase where the chest iscompressed and a relaxation or decompression phase where the chest isallowed to return to its normal position. The methods and devices of theinvention may be used in connection with any method of CPR in whichintrathoracic pressures are intentionally manipulated to improvecardiopulmonary circulation. For instance, the present invention may beused in connection with standard, manual, closed-chest CPR, interposedabdominal counterpulsation CPR, with a mechanical resuscitator, such asthe Michigan Instruments “Thumper”, with ACD-CPR, with “Lifestick” CPR,and the like. In addition, certain embodiments may be used to induceinspiration and/or coughing. This may help to maintain blood pressureduring cardiac arrest and may help patients that are incapable ofvoluntary inspiration or coughing.

[0077] In a broad sense, one aspect of the present invention providesfor stimulating contraction of at least some of the respiratory musclesduring the relaxation or decompression phase of CPR to enhance andsustain the duration of negative intrathoracic pressure during therelaxation or decompression phase. The significance of the increase innegative intrathoracic pressure during the relaxation or decompressionphase is that more venous blood is forced into the chest from theperipheral venous vasculature. As a result, more blood is allowed to beoxygenated and more blood is forced out of the chest during the nextcompression. Upon contraction of the respiratory muscles, the patientwill typically “gasp”. The invention thus provides techniques forconsistently inducing a “gasp” after chest compression.

[0078] The decrease in intrathoracic pressure produced by electricalstimulation of the inspiratory muscles, including the diaphragm, duringthe chest relaxation phase of CPR is associated with an increase incoronary perfusion pressure and thus an increase in blood flow to theheart. The coronary perfusion pressure to the heart during thedecompression phase can be calculated by the mathematical differencebetween the aortic and right atrial pressure. Right atrial pressure islowered by inspiratory effort, and therefor the aortic-right atrialgradient or the coronary perfusion pressure is increased by stimulationof inspiratory effort.

[0079] The respiratory muscles that may be stimulated to contract toenhance ventilation and/or to alter intrathoracic pressures include thediaphragm, the chest wall muscles, including the intercostal muscles andthe abdominal muscles. Specific chest wall muscles that may bestimulated to contract include those that elevate the upper ribs,including the scaleni and sternocleidomastoid muscles, those that act tofix the shoulder girdle, including the trapezii, rhomboidei, andlevatores angulorum scapulorum muscles, and those that act to elevatethe ribs, including the serrati antici majores, and the pectoralesmajores and minores as described generally in Leslie A. Geddes,“Electroventilation-A Missed Opportunity?”, Biomedical Instrumentation &Technology, July/August 1998, pp. 401-414, the complete disclosure ofwhich is herein incorporated by reference. Of the respiratory muscles,the two hemidiaphragms and intercostal muscles appear to be the greatestcontributors to inspiration and expiration.

[0080] The invention provides a variety of ways to stimulate respiratorymuscle contraction so that the magnitude and extent of negativeintrathoracic pressure during the relaxation or decompression phase maybe increased. Preferably, the respiratory muscles are stimulated tocontract by transcutaneous or transtracheal electrical field stimulationtechniques. For example, to stimulate the diaphragm, the phrenic nervemay be stimulated in the neck region near C3-C7, such as between C3, C4or C5, or where the phrenic nerves enter the diaphragm. Alternativetechniques for stimulating diaphragmatic contraction include magneticfield stimulation of the diaphragm or the phrenic nerve. Magnetic fieldstimulation may also be employed to stimulate the chest wall muscles.Electrical field stimulation of the diaphragm or the chest wall musclesmay be accomplished by placing one or more electrodes on the skin,preferably in the vicinity of the neck or the lower rib cage (althoughother locations may be employed) and then providing an electricalvoltage gradient between electrodes that induces transcutaneous currentflow to stimulate the respiratory muscles to contract. Still further,subcutaneous electrodes may also be used to stimulate respiratory musclecontraction.

[0081] In another broad aspect of the invention, venous return may beenhanced by compressing the abdomen. For example, downward compressionprovided to the abdomen causes the diaphragm to move upward into thethoracic cavity. As the abdomen is compressed, venous blood isphysically forced out of the abdominal cavity and into the thoraciccavity. Advantageously, when the abdomen is compressed, there is anincrease in resistance to the flow of blood from the thoracic aorta intothe abdominal aorta. This gradient causes a greater proportion ofarterial blood flowing to the brain and to the heart. In one aspect,abdominal compression may start during the second half of thedecompression phase and last until the compression phase or about halfway through the compression phase. The use of abdominal compressionduring CPR is described generally in J. M. Christenson, et. al.,“Abdominal Compressions During CPR: Hemodynamic Effects of AlteringTiming and Force”, The Journal of Emergency Medicine, Vol 10, pp257-266, 1992, the complete disclosure of which is herein incorporatedby reference.

[0082] According to the invention, one way to contract the abdominalmuscles is by electrical stimulation. For example, one or moreelectrodes may be positioned on the abdominal area at a variety oflocations, including the back. Hence, the abdominal muscles may be madeto contract at specific time intervals in relation to chest compressionand/or inspiratory muscle electrical stimulation. As the abdominalmuscles are electrically stimulated, the abdominal cavity squeezes toforce the diaphragm upward into the thoracic cavity. Also, venous bloodis moved from the abdomen to the thorax, and right atrial pressureincreases. In this manner, venous blood is actively transported to thethorax. Further, when abdominal compression extends into the compressionphase of CPR, exhalation is transformed from a passive to a more activeprocess. Further, an increase in coronary perfusion pressure isobtained.

[0083] The techniques employed to stimulate the inspiratory musclesand/or nerves and to stimulate the abdominal muscles may be utilizedeither alone or in combination. These stimulation techniques may also beused with or without active chest compression. For example, even in theabsence of active chest compression, large swings in intrathoracicpressure induced by electrical stimulation of the inspiratory musclesand/or nerves either alone or concomitantly with abdominal musculaturestimulation will enhance vital organ perfusion and increase the chancesfor resuscitation.

[0084] The inspiratory muscles and/or nerves are preferably stimulatedto contract immediately after the chest is compressed. Preferably, theinspiratory muscles and/or nerves are stimulated in a manner such thatas soon as the compression phase is over, the intrathoracic pressurefalls secondary to electrical stimulation of the inspiratory muscles.The compression phase may be configured to last approximately 50% of theCPR cycle. However, in some cases it may be desirable to shorten thecompression phase and lengthen the decompression phase to furtherenhance venous return.

[0085] Abdominal compression and/or abdominal musculature stimulationmay occur mid-way through the decompression phase and continue throughat least the beginning of the compression phase. As previouslydescribed, at the end of the compression phase, intrathoracic pressureis lowered to enhance venous blood return. This may be augmented bycausing the respiratory muscles, including the diaphragm, to contract.As the abdomen is compressed or the abdominal muscles are stimulated tocontract mid-way through the decompression phase, the diaphragms arepushed actively upward into the thorax to force respiratory gases out ofthe chest and venous blood is forced into the thorax. When thecompression phase is reached and the abdomen is still contracted, thereis an increase in resistance to the flow of blood from the thoracicaorta into the abdominal aorta. This gradient causes a greaterproportion of arterial blood flowing to the brain and to the heart.

[0086] In one aspect of the invention, the abdominal muscles may bestimulated sequentially in a valve-like manner so as to squeeze venousblood out of an area. For example, two electrodes may be spaced-apartfrom each other to form an electrode pair. Multiple pairs may bepositioned lengthwise on the patient. The pairs of electrodes may besequentially actuated, beginning from a bottom pair, to force blood outof the abdominal area into the thoracic cavity. Alternating the patternin which the electrodes are actuated may help to prevent muscle fatigue.

[0087] The respiratory and abdominal muscle stimulation techniques ofthe invention may be used in connection with or in close associationwith various other techniques designed to treat or diagnose the patientreceiving CPR. For example, during the relaxation or decompressionphase, the patient's airway may be occluded to prevent foreign (outside)air or respiratory gases from flowing to the patient's lungs. In thisway, the magnitude and duration of negative intrathoracic pressureduring the relaxation or decompression phase are further enhanced.Exemplary devices and methods for occluding the patient's airway duringthe relaxation or decompression phase are described in U.S. Pat. Nos.5,551,420 and 5,692,498 and co-pending U.S. application Ser. No.08/950,702, previously incorporated herein by reference. As anotherexample, the respiratory muscle stimulation techniques of the inventionmay be used in connection with ACD-CPR where the patient's chest isactively lifted during the relaxation or decompression phase to furtherenhance and sustain the duration of negative intrathoracic pressureduring the relaxation or decompression phase.

[0088] The electrodes employed by the invention to stimulate respiratorymuscle contraction may optionally be coupled to a defibrillator todeliver a defibrillation shock to the heart, or to supply energy toinitiate transthoracic or transhacheal cardiac pacing. Since the deviceis preferably in contact with the skin, the device may optionallyinclude various sensors to monitor various physiological parameters. Forexample, the device may include oxygen sensors, temperature sensors, orsensors to monitor O₂ saturation. Further, sensors may be provided tosense surface cardiac electrograms. The device may also be employed todeliver drugs transcutaneously.

[0089] In one embodiment, an adhesive compressive pad is placed over thelower portion of the sternum. Compressions are applied as with standardmanual CPR to a depth of about two to three inches. A sensor isincorporated in a compression region of the pad and is employed tosignal the triggering of respiratory muscle contraction. Preferably,portions of the compressive pad are electrically active to stimulatediaphragmatic and/or chest wall muscle contraction upon receipt of asignal from the sensor. In one aspect, the stimulator may emit a signal,such as an audible signal, a visual signal or the like, allowing therescuer to time chest compressions based on the emitted signal.

[0090] The invention also provides techniques for increasing blood flowto the thorax for non-CPR applications. For example, in certainembodiments, the invention provides for stimulation of the phrenic nerveat the cervical vertebrae to cause diaphragmatic contraction, therebyincreasing the magnitude and duration of negative intrathoracicpressure. To further increase the magnitude and duration of negativeintrathoracic pressure, a valve is employed to prevent the flow ofrespiratory gases to the lungs during at least a portion of the timewhen the diaphragm is contracting. Examples of such valves are describedin U.S. Pat. Nos. 5,551,420 and 5,692,498 and co-pending U.S.application Ser. No. 08/950,702, previously incorporated herein byreference. Such techniques are particularly useful when treatingpatients suffering from hemorrhagic shock, hypovolemic shock,cardiogenic shock, post resuscitation pulseless electrical activity,right ventricular failure, and the like. Merely by way of example, thephrenic nerve may be stimulated as follows: for hemorrhagic shock, about5 to about 30 times per minute; for hypovolemic shock, about 5 to about30 times per minute; for cardiogenic shock, about 5 to about 80 timesper minute; for pulseless electrical activity, about 5 to about 60 timesper minute. Typically, the valve will be controlled so that respiratorygases are prevented from reaching the lungs as the diaphragm begins tocontract so that the negative intrathoracic pressure will reach at least−5 mmHg to about −30 mmHg. At this time, the valve may be opened topermit gases to reach the lungs. Further, a sensor may be employed tosense the pressure within the thorax. A feedback signal from the sensormay then be employed to control the electrical signal sent to theelectrodes so that the negative intrathoracic pressure may be maintainedat optimal levels.

[0091] The techniques employed to increase the return of blood to thethorax may find particular use when treating patients suffering shockdue to gunshot wounds, and may also be used for patients who suffer froma severe myocardial infarction and shock. Presently available drugs areunable to provide such a function.

[0092] Phrenic nerve stimulation may also be used to electricallyventilate a patient. Such a process is particularly useful inapplications where intubation is undesirable or when positive pressureventilation can cause difficulties with bursting of pulmonary alveoliand bronchioles.

[0093] One way to stimulate the phrenic nerve (for each of theapplications described above) is with the use of one or more electrodesthat are placed on the patient's neck, preferably at the C3 to C7 regionof the cervical vertebrae, and more preferably at the C3 to C5 region.In one aspect, the electrode may be placed both anterior and posterior.Further, a multiphase wave form, such as a biphasic waveform, includingasymmetrical biphasic waveforms, may be employed. Such a configurationis particularly useful in reducing the amount of power required,reducing muscle fatigue, and increasing tidal volume (duringventilation).

[0094] Depending on the particular treatment, the electrical signal mayhave a wide range of currents, a wide range of frequencies, and a widerange of pulse widths. Merely by way of example, electrical current maybe used that is in the range from about 100 milliamps to about 2,000milliamps at a frequency in the range from about 10 Hz to about 100 Hz,and in pulse widths in the range from about 1 μs to about 5 ms.

[0095] Referring now to FIGS. 1 and 2, an exemplary embodiment of adevice 10 to provide respiratory muscle contraction during theperformance of CPR will be described. Device 10 comprises a compressionmember 12 which is configured so that it may be received over thepatient's chest in the area of the sternum. In this way, compressionmember 12 may be pressed downward to compress the patient's chest duringthe compression phase of CPR. Coupled to compression member 12 by a pairof arms 14 and 16 are a pair of end elements 18 and 20, respectively. Asbest shown in FIG. 3, end element 18 includes an electrode 22 on abottom surface, it being appreciated that end element 20 or compressionmember 12 may include a similar electrode. Electrode 22 may comprise anadhesive electrically active pad, such as an R2 pad, commerciallyavailable from 3M. Electrodes 22 may also include a conductive gel.Other electrodes that may be employed include electrodes constructed ofstainless steel, carbon-filled silicone rubber, platinum, iridium,silver silver-chloride, and the like. The electrode may be applied tothe skin surface or may pierce the skin surface. It will also beappreciated that electrode 22 may be configured to operate in amonopolar manner, a bipolar manner or a multipolar manner. Further,electrode 22 may be configured to deliver electrical stimulation atdifferent frequencies, pulse widths, pulse trains and voltage outputs tooptimize respiratory muscle stimulation. The configuration of arms 14may be varied to vary the lead vector produced by electrode 22. Forexample, the lead vector may be from one side of the chest to the other,to the midcompression region, or from one lead to the other on the sameside of the chest. Device 10 may also be configured to deliver an outputbased, at least in part, upon the chest wall impedance. An energy sourceis coupled to the electrodes to deliver low energies, e.g., less thanabout 2 amps, to stimulate the respiratory muscles.

[0096] Although electrodes 22 have been described as electrodes whichprovide electrical stimulation, it will be appreciated that device 10can be modified to provide a magnetic field to stimulate the respiratorymuscles to contract. For example, a magnetic field may be applied to thephrenic nerve to produce diaphragmatic and/or chest wall musclestimulation. As such, an upper back pad may be needed for optimalphrenic nerve stimulation.

[0097] Exemplary techniques for stimulating the respiratory muscles, andparticularly the diaphragm, to contract, including techniques forproviding both electrical and magnetic stimulation of the inspiratorymotor nerves, are described in L. A. Geddes, “Electrically ProducedArtificial Ventilation,” Medical Instrumentation 22(5): 263-271 (1988);William W. L. Glenn et al., “Twenty Years of Experience in Phrenic NerveStimulation to Pace the Diaphragm,” Pace 9:780-784 (November/December1986, Part 1); P. L. Kotze et al., “Diaphragm Pacing in the Treatment ofVentilatory Failure,” Sant. Deel 68:223-224 (Aug. 17, 1995); L. A.Geddes et al., “Inspiration Produced by Bilateral Electromagnetic,Cervical Phrenic Nerve Stimulation in Man,” IEEE Transactions onBiomedical Engineering 38(9):1047-1048 (October 1991); L. A. Geddes etal., “Optimum Stimulus Frequency for Contracting the Inspiratory Muscleswith Chest-Surface Electrodes to Produce Artificial Respiration,” Annalsof Biomedical Engineering 18:103-108 (1990); Franco Laghi et al.,“Comparison of Magnetic and Electrical Phrenic Nerve Stimulation inAssessment of Diaphragmatic Contractility,” American PhysiologicalSociety, pp. 1731-1742 (1996); and William W. L. Glenn et al.,“Diaphragm Pacing by Electrical Stimulation of the Phrenic Nerve,”Neurosurgery 17(6):974-984 (1985). The complete disclosures of all thesereferences are herein incorporated by reference in their entirety. Theelectrodes of the invention may be configured to operate in a monopolarmanner, a bipolar manner, or a multi-polar manner.

[0098] Arms 14 and 16 are preferably constructed of a flexible material,including fabrics, such as a nylon fabric, elastomeric materials,including rubbers, plastics and the like, to facilitate proper placementof electrodes 20 on the patient. Optionally, arms 14 and 16 may bepivotally attached to compression member 12 to allow electrodes 20 to beplaced at a variety of locations on the patient.

[0099] As illustrated in FIG. 4, a top side of end element 18 includes ametronome 24. Metronome 24 assists the rescuer in performing regularchest compressions when performing CPR by emitting regular audible orvisual signals. This, in turn, aids in the coordinated timing betweenthe compression of the chest and the stimulation of the respiratorymuscles during the relaxation or decompression phase. End element 18further includes a voltage controlling mechanism, such as apotentiometer 26, which enables the rescuer to change the voltage outputof electrode 22 (see FIG. 3) to ensure adequate diaphragmaticstimulation. In one alternative, proper voltage may be determinedautomatically depending upon chest wall impedance that is measured witha impedance meter. In this way, device 10 may be configured so that itdoes not over stimulate or under stimulate the inspiratory motor nerves.End element 18 still further includes an energy source 28 which providesenergy to the various electrical components, sensors, impedance meters,electrodes, and the like of device 10. Energy source 28 may convenientlycomprise a battery that is stored within end element 18. Alternatively,a wide variety of external energy sources may be employed to operatedevice 10. For example, electrical energy may be provided by aventilator which is employed to ventilate the patient, a defibrillatorwhich may optionally be employed to provide defibrillation andtransthoracic cardiac pacing and house the electrical components of asensing system, an electrical generator which converts mechanical energyprovided by the rescuer during compression of compression member 12 toelectrical energy, and the like.

[0100] Although not shown, device 10 may optionally include a variety ofdisplays, instructions for use, and controls that may be located oncompression member 12 , arms 14 or end elements 18. For example, device10 may include a force, pressure or depth display which displays theamount of force, pressure or depth being applied to compression member12 by the rescuer. In this way, the rescuer may be provided withinformation regarding the amount of force being supplied to compressionmember 12 . Preferred force ranges may be included on device 10 so thatthe rescuer may determine if he is within a recommended force range.Device 10 may also include a compression counter display which displaysthe number of compressions experienced by compression member 12. Thecompression counter may be configured to display cycles of compressionsto allow the rescuer to visualize the number of compressions that areperformed for every respiratory muscle stimulation. Device 10 may stillfurther include a surface electrogram sensing display to displayinformation relating to a surface electrogram. Still further, aphysiological parameter display may be provided to display variousphysiological parameters such as O₂ saturation, CO₂ saturation, skintemperature, and the like.

[0101] As shown in FIG. 5, device 10 may be provided with a wishboneconfiguration so that end elements 18 are placed over the lower marginof the rib cage. Arms 14 and 16 may be configured to be fixedly mountedrelative to compression member 12 so that the electrodes will always beplaced at about the same region on the chest. Alternatively, arms 14 and16 may be movably mounted to compression member 12 so that the positionof the electrodes on the patient may be adjusted. As previouslydescribed, arms 14 and 16 may be configured to be constructed of eithera flexible or a rigid material to facilitate proper placement of theelectrodes on the patient.

[0102] In another embodiment illustrated in FIG. 5A, a device 10′ isprovided which is similar to device 10 of FIG. 5 (with similar elementsbeing labeled with the same reference numerals) and further includes anarm 14 a having an end element 18 a which is placed over the left axillaand has an electrode for defibrillation between the arm and the chest.In this way, compression member 12 may be placed over the sternum, withend elements 18 and 20 being placed over the lower rib cage to stimulatethe respiratory muscles to contract between chest compressions aspreviously described. When needed, defibrillation may be provided byactuating the electrode on end element 18 a. Optionally, adefibrillation unit 52 a may be coupled to device 10′ . Unit 52 aincludes an energy source for both diaphragmatic pacing anddefibrillation. In this way, the energy source and other electricalcomponents may be included within device 10′ or in unit 52 a.

[0103] Referring now to FIG. 6, a schematic diagram of the electricalcomponents employed with device 10 will be described. Electrical poweris provided to the various components with a circuit supply voltagemodule 30. Module 30 corresponds to energy source 28 of FIG. 4 and maycomprise an internal or external power supply as previously described. Acompression sensor and force display module 32 is provided to sensecompression of compression member 12 (see FIG. 1) and to optionallydisplay the force, pressure, and/or depth information to the rescuer.Exemplary compression sensors that may be employed include piezoelectriccrystals that produce an electrical charge in proportion to the amountof force applied, fluid reservoirs and associated pressure sensors todetect an increase in pressure upon application of a force, straingauges, and the like. Conveniently, the force detected by thecompression sensor may be displayed on an LCD, LED or other display ondevice 10.

[0104] A compression counter/display and signal control module 34 iscoupled to compression sensor 32 and counts each compression ofcompression member 12. The number of compressions may conveniently bedisplayed on device 10. Signals from module 34 are also transferred to astimulation control and pulse sequence generator module 36 which isresponsible for producing electrical signals employed by electrodes 22(see FIG. 3). Module 36 is configured to produce an electrical pulseimmediately after receipt of a counting logic signal from module 34. Inthis way, the electrodes may be actuated immediately after thecompressive force is applied by the rescuer so that respiratory musclestimulation is triggered to occur at the beginning of the relaxation ordecompression phase of CPR. Module 36 preferably includes a signalgenerator to produce pulsed sequences resulting in the delivery ofenergy through the electrodes. Module 36 may be configured to producepulses which correlate to every signal received from module 34 or onlyfor selected signals from module 34. In this way, respiratory musclestimulation may occur immediately after every compression or only aftercertain compressions.

[0105] In electrical communication with module 36 is a high voltagemodule 38 which functions to provide high voltage and/or high currentwaveforms so that the electrodes may operate at the proper stimulationvoltage and/or current level. Module 38 may be employed to operate theelectrodes to provide respiratory muscle stimulation as shown. Theapplied voltage and/or current may be modified by the rescuer byoperating potentiometer 26 (see FIG. 4). Additionally, module 38 may beemployed to operate the electrodes so that they perform a defibrillationfunction or to accomplish transthoracic cardiac pacing as is known inthe art. In this way, device 10 may be used to stimulate the respiratorymuscles to contract during CPR as well as for cardiac defibrillation ortransthoracic cardiac pacing.

[0106] Also in electrical communication with module 34 is a ventilationcontrol module 40. Module 40 is optional and may be provided to receiveelectrical signals from module 34 indicating actuation of compressionsensor 32. Module 40 is coupled to a ventilation device 42 which may beconfigured to periodically ventilate the patient in an automated mannerbased on actuation of compression sensor 32 as CPR is being performed.Preferably, module 40 will be configured to actuate the ventilator at afrequency of about one ventilation to every five compressions. As oneexample, control module 40 may be constructed similar to the moduledescribed in U.S. Pat. No. 4,397,306 to coordinate the actuation ofventilation device 42 with actuation of compression sensor 32. Thecomplete disclosure of this reference is herein incorporated byreference. Although device 10 has been described as being coupled to anautomated ventilation device, it will be appreciated that manualventilation devices and techniques may also be employed to ventilate thepatient during the performance of CPR, whether or not electricallycoupled to device 10. One advantage of providing ventilation controlmodule 40 is that ventilation device 42 and high voltage/high currentcontrol module 38 are electrically coupled so that coordination ofventilation, diaphragmatic pacing, cardiac pacing, and/or defibrillationmay occur.

[0107] Device 10 may be modified so that the electrical components (suchas those set forth in FIG. 6) and power source are provided in aseparate unit. For example, such components may be incorporated into adefibrillator which in turn is coupled to device. In this way, device 10may be manufactured relatively inexpensively, with the electricalcomponents being provided in a separate unit. Further both diaphragmaticstimulation and pacing may be provided with a base unit which is coupledto device 10.

[0108] In one particular alternative, patient ventilation may beassisted with the use of a ventilation device having a thresholdnegative intrathoracic pressure device which opens when a predeterminednegative intrathoracic pressure is reached during the relaxation ordecompression phase as described in U.S. Pat. Nos. 5,692,498 and5,551,420, previously incorporated by reference. With such aconfiguration, device 10 may be provided with a controller which iscoupled to the threshold valve so that actuation of the threshold valvemay be coordinated with diaphragmatic stimulation to optimize thenegative intrathoracic pressure. In particular, the impedance thresholdvalve may be opened and closed using a servo- orelectromagnetically-controlled circuit that is coupled to device 10 sothat its operation may be coordinated with operation of the electrodes.

[0109] Still referring to FIG. 6, a metronome timing display module 44is electrically coupled to circuit supply high voltage/high currentmodule 30 and is employed to produce regular audible and/or visualsignals to assist the rescuer in performing regular chest compressions.A surface electrogram sensing/display module 46 is also electricallycoupled to module 30 and allows for the sensing of surface electrogramsand displaying the sensed information. Exemplary sensors for sensingsurface electrograms include needles that are inserted through the skin,electrode-gel coupled sensors, and the like. A gas sensing displaymodule 48 is provided to sense and display the amount of various gasesin a patient's blood, airway, or skin/cutaneous surface. For example,module 48 may be employed to sense the amount of oxygen saturation, CO₂saturation, and the like. Optionally, module 48 may include a thermistoror thermocouple-based temperature measuring device that may be placedagainst or inserted into the skin to measure the patient's bodytemperature.

[0110] A drug delivery control module 50 may optionally be provided tosupply various drugs to the patient. For example, module 50 may be apassive device for delivering nitroglycerine. Alternatively, module 50may be an active device for electrophoretic delivery of drugs such asvasopressin, an anti-arrhythmic drug, and the like. In this way, module50 provides device 10 with the ability to transcutaneously deliver drugsas device 10 is placed against the patient's body to perform CPR.

[0111] Although one embodiment illustrates the use of a compressionmember to sense when the chest is being compressed, it will beappreciated that other techniques may be provided to sense chestcompression. For example, electrodes may be placed on the chest andsensors employed to detect electrical impulses or a change in impedanceas the chest is compressed. Alternatively, a pressure sensor may beprovided in an airway device to detect an increase in airflow in thepatient's airway. The electrodes may be coupled to an externaldefibrillator-pacer that is capable of delivering low energies, i.e.about 0.01 amps to about 2 amps, and more preferably about 0.1 amps toabout 2.0 amps, to stimulate the diaphragm or other respiratory muscles.In this way, a system is provided which may provide respiratory musclestimulation (that is coordinated with chest compressions), pacing, anddefibrillation.

[0112] Referring now to FIG. 7, an exemplary method for performing CPRusing device 10 will be described. As shown, device 10 is placed on thepatient such that compression member 12 is placed over the sternum andend elements 18 and 20 are placed over the ribs. As previouslydescribed, the particular location and arrangement of end elements 18and 20 may be varied to optimize respiratory muscle stimulation. Therescuer then compresses compression member 12, preferably by placingboth hands on compression member 12 and pushing downward. Compression ofcompression member 12 proceeds in a manner similar to that performedwhen performing traditional CPR. Immediately after the maximumcompression is applied, electrodes on end elements 18 and 20 areactuated to stimulate the diaphragm and/or the chest wall muscles tocontract during the relaxation or decompression phase. Conveniently,power is supplied to the electrodes via an external defibrillator 52,although other energy sources may be employed as previously described.The electrodes may be actuated during every relaxation or decompressionphase or during only selected relaxation or decompression phases,depending on the need of the patient. Since device 10 is coupled to thedefibrillator 52, the patient may also be supplied with a defibrillationshock or cardiac pacing. Hence, defibrillator 52 may be used tostimulate respiratory muscle contraction as well as to pace and/ordefibrillate the heart. In that case, the sensor may be configured to bethe same electrodes used to defibrillate the patient so that nocompression member would be needed.

[0113] To stimulate respiratory muscles to contract, the currentsupplied by the electrodes is preferably in the range from about 0.01amps to about 2.5 amps, and more preferably from about 0.1 amps to about1.0 amps. However, it will be appreciated that the specific amount ofcurrent will depend on chest wall impedance and mode of stimulation,e.g., square wave impulse, unipolar wave forms, biphasic wave forms,multiphasic wave forms, multi-vectorial pathways, use of pulse trains,and the like. In some cases it may be desirable to stimulate one side ofthe diaphragm or chest wall at a different time from the other side ofthe diaphragm or chest wall, e.g., by about 10 msec to about 200 msec,to reduce the risk of shock to the rescuer and to reduce inspiratorymuscle fatigue. The respiratory muscles may be stimulated to contract ata frequency in the range from about 30 to about 120 times per minute.The timing sequence for stimulating different chest wall or other sitesto induce inspiratory muscle contraction may be alternated to avoidmuscle fatigue by varying the amplitude and duration of stimulationbased upon a resistance or impedance measurement at any givenstimulation site. Resistance measurements may be used in a closed loopcircuit to help vary stimulation site location and stimulation outputs.

[0114] Periodically, about every one to ten compressions, the patient isventilated. Ventilation may be accomplished using an automatedventilator which may or may not be coupled to device 10. Alternatively,various manual ventilators may be employed as is known in the art. Inone particular embodiment, a ventilation device is coupled with athreshold valve so that the duration and extent of negativeintrathoracic pressure may be controlled during the relaxation ordecompression phase as previously described. A pressure sensor andfeedback loop circuit may also be used to measure the negativeintrathoracic pressure in the airway and adjust the energy delivered tothe electrode to maintain a generally constant negative intrathoracicpressure caused by each contraction of the respiratory muscles.

[0115] Referring now to FIG. 8, an alternative embodiment of a device 54for stimulating the respiratory muscles to contract will be described.Device 54 comprises an endotracheal tube 56 having an inflatable member58 (shown in phantom line) which serves to secure endotracheal tube 56in the patient's airway as is known in the art. Endotracheal tube 56includes a lumen 60 through which the patient is ventilated. Device 54further includes a pair of electrodes 62 and 64 which operate in abipolar manner to electrically stimulate the phrenic nerve, althoughother numbers and arrangements of electrodes may be employed, includingmonopolar electrode configurations. Electrode 62 or a plurality ofelectrodes may also be attached to inflatable cuff 58 as shown in FIG.8B. In turn, stimulation of the phrenic nerve causes the diaphragm andchest wall muscles to contract. An electrical lead 66 is provided tosupply electrical current to electrode 62.

[0116] In this way, when device 54 is inserted into the patient'sairway, electrodes 62 and 64 are positioned so that when current issupplied to electrode 62, the phrenic nerve is electrically stimulatedto cause the diaphragm muscles to contract. As with other embodimentsdescribed herein, electrode 62 is preferably actuated during therelaxation or decompression phase of CPR so that the respiratory musclescontract to increase the magnitude and extent of negative intrathoracicpressure during the decompression phase. Optionally, lead 66 may becoupled to a controller of a compression device which is similar tocompression member 12 so that electrical stimulation of the phrenicnerve may be coordinated with chest compression. In a similar manner,lead 66 may be coupled to a ventilator which supplies air through lumen60 so that ventilation may also be coordinated in a manner similar tothat described with previous embodiments. Further, an impedance valvemay be coupled to the endotracheal tube as described in U.S. Pat. Nos.5,551,420 and 5,692,498, previously incorporated by reference.

[0117] In another alternative, endotracheal tube 54 may be provided withelectrodes to also pace the heart. Such electrodes may be configured ina bipolar or monopolar manner, and may optionally be connected with anexternal electrode or an esophageal electrode.

[0118] Although described in the context of an endotracheal tube, itwill be appreciated that electrical stimulation of the phrenic nerve maybe accomplished by placing electrodes on a laryngeal mask airway, orother ventilation device which is placed within the larynx, esophagus,or trachea. Further, one or more electrodes may be included on alaryngeal mask airway or endotracheal tube that is inserted into theesophagus to pace the heart and/or to stimulate the phrenic nerve. Asone example, such an electrode may be placed on an airway as describedin U.S. Pat. No. 5,392,774, the disclosure of which is hereinincorporated by reference. As another alternative, an electricalstimulator may be placed externally over the neck to stimulate thephrenic nerve. In still a further alternative, a magnetic field may beproduced about the phrenic nerve to stimulate the diaphragm or chestwall muscles to contract. Devices for producing such an electrical fieldmay be placed within the airway or externally about the neck.

[0119] One particular embodiment of a device 200 for either electricallyor magnetically stimulating the phrenic nerve is illustrated in FIG. 8A.Device 200 comprises a collar having one or more electrodes or elementsto produce electrical current or a magnetic field to stimulate thephrenic nerve. Device 200 is coupled to a controller 202 having a powersource. Also coupled to controller 202 is a compression sensor 204 sothat respiratory muscle stimulation may be coordinated with chestcompressions as previously described.

[0120] In one alternative, the collar of device 200 may comprise a typeof collar commonly used to rapidly stabilize the neck and/or help totilt the head backwards. For example, such collars are often used intrauma situations to provide stability or to open a patient's airway.Such a collar may include at least two electrodes that are positionedsuch that they are anterior and posterior to the cervical vertebrae C3to C6 when the collar is secured about the patient's neck. Theseelectrodes may then be coupled to controller 202 to stimulate thephrenic nerve according to any of the techniques described herein.

[0121] In one particular embodiment, the invention may employ the use ofa mechanical chest compressor which is coupled to a ventilator asdescribed in U.S. Pat. No. 4,397,306, previously incorporated byreference. The stimulating electrodes may be coupled to the chestcompressor or ventilator via a controller so that the controller maycoordinate chest compression, ventilation, respiratory musclestimulation, defibrillation, pacing, as well as other featurespreviously described. Further, the amount of negative intrathoracicpressure generated with each contraction of the respiratory muscles maybe used to adjust the energy needed for subsequent contractions. Such asystem may conveniently be located in an emergency vehicle or a healthcare facility.

[0122] For example, one such system 100 is illustrated schematically inFIG. 9 and comprises a compression piston 102 that is held over apatient's thorax 104 by a support arm 106. Compression piston 102 ispowered by an electric or pneumatic motor 108. When in use, piston 102moves downward to compress the patient's chest. After the compressionphase is complete, a spring 110, or other return mechanism, lifts piston102 from the patient's chest to maximize the negative intrathoracicpressure during the relaxation phase. A controller is included withmotor 108, and piston 102 includes a sensor 112 so that the respiratorymuscles may be triggered to contract during the relaxation ordecompression phase. The controller may optionally be coupled to aventilator, a defibrillator, a heart pacer, a drug delivery system,various other sensors and/or an airway occluding device as previouslydescribed.

[0123] Still another embodiment of a device 300 for stimulating therespiratory muscles to contract is illustrated in FIG. 10. Device 300comprises an insulated blanket 302 which is constructed of anelectrically insulative material, such as rubber, to protect the rescueragainst possible shocks. Blanket 302 may incorporate any of the elementsof other embodiments described herein to assist in respiratory musclestimulation, monitoring, drug delivery, sensing, defibrillation, pacing,and the like. For example, blanket 302 includes electrodes 304 which maybe selectively located to stimulate respiratory muscle stimulation. Forexample, electrodes 304 may be placed over the lower margin of the ribcage as previously described, or over the abdomen to stimulate theabdomen. A compression sensor 306 is provided to coordinate chestcompressions with activation of electrodes 304. A potentiometer 308 isincluded to regulate the amount of current supplied by electrodes 304. Apower supply 310 is farther provided to supply current to electrodes304.

[0124] Referring now to FIG. 11, a stimulation system 320 will bedescribed. System 320 includes multiple leads 322-332 that are arrangedin pairs. Although shown with six leads, it will be appreciated thatother numbers and arrangements may be employed. For example, leads maybe placed onto the patient's back. Leads 322-332 are arranged so thatpairs of the leads may be sequentially actuated to produce a wave ofcontractions forcing venous blood back into the thorax and causing thediaphragm to be pushed upward to lead to respiratory gas exhalation. Forexample, leads 330 and 332 may first be actuated, followed by actuationof leads 326 and 328, and followed by actuation of leads 322 and 324.

[0125] The leads are coupled to a controller/power source 334 to supplycurrent to the leads and to control when the leads are actuated.Conveniently, controller 334 may be configured similar to thecontrollers and/or other electrical circuitry that are associated withthe various inspiratory muscle stimulator systems described herein. Insome cases, controller 334 may be incorporated into or coupled withthese inspiratory stimulation controllers and/or electrical circuitry tocoordinate alternating inspiratory muscle and abdominal musculatorycontraction. Further, such a controller may be configured to control thetiming sequence of the leads so that the abdominal stimulation occursabout half way into the inspiratory muscle stimulation phase. Thistypically occurs about half way into the chest wall decompression phasewhen chest compressions are performed.

[0126]FIGS. 12, 12A and 12B illustrate devices or systems used tosimultaneously cause an increase in intra-abdominal pressure andtransient airway occlusion to induce an electrical cough, therebypromoting blood out of the chest to the brain and out of the abdomen tothe chest. When performed in connection with chest compressions, cardiacoutput is maintained by rhythmically increasing intrathoracic pressureagainst a closed airway with a simultaneous increase in abdominalpressure. Upon release of the abdominal stimulation and expiratoryairway occlusion, followed by passive or active downward movement of thediaphragm, the chest is filled with air and both ventilation andcardiopulmonary circulation is induced.

[0127] Shown in FIG. 12 is a system 350 to produce a cough by periodicocclusion of respiratory gases and by abdominal stimulation. System 350includes a respiratory face mask 352 having a pressure release valve 353to transiently prevent respiratory gases from exiting the lungs to raiseintrathoracic pressure. System 350 further includes one or morestimulation electrodes 354 that may be employed to stimulate inspiratoryeffort similar to that described with previous embodiments. Althoughshown on the abdomen, it will be appreciated that electrodes may beplaced at other locations, such as on the neck or chest, to alsostimulate the diaphragm to contract. Positioned between electrodes 354and release valve 353 is a controller 356. In this way, opening ofrelease valve 353 may be coordinated with actuation of electrodes 354.Also shown in FIG. 12 is a chest compression site 358 to indicate wherechest compressions may optionally be performed. System 350 mayoptionally include a respiratory air bag 360 to periodically ventilatethe patient.

[0128] In use, valve 353 is closed to prevent respiratory gases fromexiting the patient. Electrodes 354 are actuated to increaseintra-abdominal pressure. During stimulation of the abdominal muscles,valve 353 is abruptly opened to induce the patient to cough. In oneaspect, valve 353 may be opened for a time in the range from about 10 msto about 500 ms after the abdominal muscles are stimulated to contract.After coughing, air bag 360 may be used to ventilate the patient. Chestcompressions and/or respiratory muscle stimulation may optionally beperformed prior to each induced cough.

[0129] Referring now to FIG. 12A, mask 352 will be described in greaterdetail. Coupled to mask 352 are a pair of straps 362 that may be securedtogether about the patient's head to seal mask 352 to the patient'sface. Conveniently, a material, such as Velcro, may be employed to holdthe straps together. Extending from mask 352 is an expiration tube 366which is coupled to valve 353. Also coupled to valve 353 is a connector368 to allow valve 353 to be coupled to controller 356. Valve 353 mayinclude an actuator that runs on DC voltage so that when an electricalsignal is sent from controller 356, valve 353 is opened. Valve 353further includes an expiratory gas port 368 to allow respiratory gasesfrom the patient to be exhaled once valve 353 is opened.

[0130] Mask 352 also includes a pressure transducer port 370 which mayinclude a pressure transducer to monitor the pressure within thepatient. The transducer may be coupled to controller 356 (see FIG. 12 )so that the pressure may be monitored. Mask 352 may further includes asafety pressure release check valve 372 that may be configured to openif the intrathoracic pressure becomes too great. Coupled to tube 366 isa ventilation bag valve connector 374 that allows air bag 360 (see FIG.12 ) to be coupled to mask 352.

[0131]FIG. 12B illustrates an endotracheal/abdominal stimulation system376. System 376 includes one or more electrodes 378 positioned on theabdomen to stimulate the abdominal muscles. An endotracheal tube 380 isalso provided with one or more electrodes 382 to stimulate the diaphragmto contract. A controller 384 is provided to control actuation of bothelectrodes 378 and 382. In this way, diaphragmatic stimulation may bealternated with abdominal stimulation. Alternatively, a chestcompression site 386 may be provided. However, external chestcompressions may not be needed once an alternating inspiratory/abdominalmuscle stimulation pattern is established. System 376 may optionallyinclude a valve system 388. Valve system 388 may include a pressurerelease valve similar to valve 353 of FIG. 12A to induce the patient tocough. Valve system 388 may optionally include a threshold impedancevalve and/or a threshold expiration valve similar to the valvesdescribed in U.S. Pat. Nos. 5,551,420 and 5,692,498 to augment negativeand/or positive negative intrathoracic pressures. In this way, largeincreases and/or decreases in intrathoracic pressures may be obtained.System 376 may also optionally include a respiratory bag 390 toperiodically supply respiratory gases to the patient.

[0132] Hence, in one aspect, the invention may utilize either the facemask system of FIG. 12 or the endotracheal tube system of FIG. 12B toperiodically block the release of respiratory gases or to periodicallyblock both expiratory and inspiratory gases. This may be done incombination with abdominal and/or diaphragmatic muscle stimulation.Chest compressions may also be performed, but may not be needed if analternating inspiratory/abdominal muscle stimulation pattern isestablished.

[0133] Referring now to FIG. 13, one embodiment of a system 400 that isparticularly useful for unilateral or bilateral stimulation of thephrenic nerve will be described. System 400 is configured tosequentially initiate an action potential to cause diaphragmaticcontractions. More specifically, system 400 is configured to initiate a“gasp” produced by contracting the diaphragm once a short durationstimulation pulse train is applied using surface electrodes. Optionally,system 400 may also be configured to electroventilate a patient byproducing long duration stimulation pulse trains with a ramped increasein voltage or current output using the electrodes, thereby producingcontrollable respiratory tidal volumes greater than 500 ml.

[0134] System 400 may conveniently be described in terms of sensing,control, and output stages. The sensing stage comprises circuitcomponents designed to sense when a chest compression is delivered tothe patient. In cases where system 400 is used for electroventilation orfor patients in shock, the sensing stage is designed to senseinspiratory effort. A variety of sensors may be employed to sense chestcompressions and inspiratory effort, including force/pressuretransducers, electromechanical switches, magnetic reed switches, and thelike. As shown in FIG. 13, system 400 utilizes a compression pad 402that houses the sensor. Compression pad 402 may be placed over thepatient's sternum upon administration of CPR. Inspiratory effort sensorsmay be located on the patient's chest or in the inspiratory impedancevalve.

[0135] One embodiment of compression pad 402 is illustrated in FIGS. 14and 15. As shown, a sensor 404 is disposed within pad 402 and includes aswitch 406 that is depressed upon compression of pad 402 during theperformance of CPR. A transmission cable 408 is coupled to sensor 404 topermit the transmission of a signal once a compression has been sensed.As best shown in FIG. 14, cable 408 is coupled to a cable connector 410that permits sensor 404 to be electrically coupled with the sensingstage circuit components of system 400. Hence, once a chest compressionis sensed, the signal is transferred via cable 408 to compression detectcircuitry 412 of system 400 to indicate that a compression has beensensed. The signal is then transferred to the control stage of system400 which includes: 1) compression count circuitry 414 to count thenumber of chest compressions, 2) stimulation delay circuitry 416 todelay initiation of the stimulation pulse, and 3) stimulation “ON” pulseduration circuitry 418 to initiate pulse duration or stimulator “ON”time. Delay circuitry 416 is configured to deliver the stimulation pulsetrain at the appropriate timing during the compression phase of CPR.However, it will be appreciated that the stimulation pulse train may bedelayed to stimulate the patient at any time during the compression ordecompression phases of CPR. Moreover, in some cases, system 400 may beconfigured to produce a repeating signal to indicate to the rescuer whento perform chest compressions. In such a case, stimulation delaycircuitry 416 would not be needed.

[0136] Pulse train duration circuitry 418 is synchronously actuated withthe delay circuitry to control the duration or pulse width of the pulsetrain. In other words, the pulse train duration controls the amount oftime the stimulator is “ON” to deliver the pulse train to theelectrodes. The pulse width of the pulse train may be adjusted tostimulate the patient during the decompression phase of CPR. However, itwill be appreciated that the pulse width may be preset and/or adjustedto stimulate the patient during any segment of the compression ordecompression phases of CPR. Further, as previously described, system400 may be used in non-CPR applications, and pulse train durationcircuitry 418 may be configured to produce an appropriate pulse trainfor the particular application.

[0137] Also actuated synchronously with stimulation delay circuitry 416and pulse train duration circuitry 418 is compression count circuitry414. Compression count circuitry 414 is configured to count the numberof chest compressions and initiate the stimulation pulse train or “ON”time during the appropriate compression/decompression cycle. Merely byway of example, the counting circuitry may be preset to stimulate at1:1,2:1, or 3:1 compressions per stimulation pulse. If 2:1 is selected,the stimulation “ON” pulse train stimulates the patient once upon everyother chest compression. If 3:1 is selected, the stimulation “ON” pulsetrain stimulates the patient once upon every third chest compression.Controlled pulse trains, once actuated to oscillate, are transferred tothe output stage of system 400 that produces an asymmetrical biphasicwave form as shown in block 420.

[0138] To produce the biphasic wave form, system 400 includes astimulator 422 that includes a frequency control oscillator 424 thatreceives the signal from pulse train duration circuitry 418. Frequencycontrol oscillator 424 is employed to control the frequency of theelectrical signal that is transferred to electrodes 427 of stimulator422. A pulse width control circuit 426 is also provided to control thepulse width of the electrical signal. A high voltage, high currentamplifier 428 and a DC-DC boost converter 430 are employed to convertthe signal to a high voltage, high current DC signal which is then sentto electrodes 427. Merely by way of example, stimulator 422 may beemployed to produce an asymmetrical biphasic wave form having a pulsewidth of about 300 microseconds, with controllable current amplificationbeing in the range of about 100 milliamps to about 2,000 milliamps.

[0139] For patients in shock, system 400 may be configured so that thepulse is activated after each breath of the patient for about 0.25 toabout 5 seconds. The ratio of breath to phrenic nerve stimulation mayvary from 2:1 to about 1:5. Further, a threshold valve may be used tocontrol the supply of respiratory gases to the lungs during treatment ofboth shock and CPR as previously described.

[0140] FIGS. 16-21 illustrate various circuit diagrams that may be usedin constructing the stimulator control portion of system 400, it beingappreciated that a variety of other circuits may be used to constructsystem 400. For example, FIG. 16 illustrates a circuit diagram of aninput control switch 500 that is used to select the type of compressionpad transducer, i.e. sensor 404 of FIGS. 14 and 15. This selection maybe for a force/pressure transducer or a microswitch.

[0141]FIG. 17 illustrates a circuit diagram of a manual switchcontroller 510 that may be used in compression detect circuitry 412 ofFIG. 13. Controller 510 functions to produce a visual light and anaudible tone when a chest compression is detected via the compressionpad. As such, controller 510 includes a switch 512 that would be housedin the compression pad of FIG. 15.

[0142]FIG. 18 illustrates a circuit diagram of an input signal anddisplay module 520 that may also be used in constructing compressiondetect circuitry 412 of FIG. 13. Module 520 functions to display thestrength of the chest compression if a force transducer is used withinthe compression pad, or displays that a chest compression occurred if amicro switch is used within the compression pad.

[0143]FIG. 19 illustrates a circuit diagram of a compressioncounter/reset module 530 that may be used in constructing compressioncount circuitry 414 of system 400. Module 530 is configured to count andreset the counter based upon the preselected compression: stimulationratio. For example, if 2:1 is selected, the circuit detects twocompressions, sends a stimulation “OK” signal to the delay circuit ofFIG. 20 and resets the counter to begin the compression countingsequence over again.

[0144] As just mentioned, FIG. 20 illustrates a sense and delay module540 that may be used to construct stimulation delay circuitry 416 ofFIG. 13. Module 540 functions to delay when the stimulator is turned“ON” in reference to the decompression phase of CPR. Module 540 is atiming circuit triggered by the compression count circuitry of module530 and may be adjusted to delay the stimulator “ON” pulse to anyportion of the CPR cycle.

[0145]FIG. 21 illustrates a stimulator ON adjust module 550 that may beused to construct pulse train duration circuitry 418 of system 400.Module 550 functions to control how long the stimulator is “ON”. Inother words, module 550 determines how long the stimulator pulse trainis delivered to the patient to stimulate the phrenic nerve.

[0146] Referring now to FIG. 22, various methods for utilizing system400 to treat a patient suffering from cardiac arrest will be described.As shown in step 432, the system is initialized by reading variouspreset parameters. The user then has the option to operate the system inmanual or automatic mode as illustrated in step 434. If manual mode isselected, the system will be configured to stimulate diaphragmaticcontraction based upon when the rescuer compresses the patient's chest.This process begins by sensing a chest compression as shown in step 436.After sensing chest compression, the production of the stimulatingcurrent is delayed for a certain preset time and is provided with acertain pulse train and pulse width as shown in step 438. Further, thechest compression is counted with a counter. The process then proceedsto step 440 where it is determined whether the counter has reached apreset value. If not, the process proceeds to step 442 where the counteris incremented and returns back to step 436 where the next chestcompression is sensed. If the counter has reached the preset value, thestimulating signal is sent to the electrodes as shown in step 442 tostimulate the phrenic nerve as illustrated in step 444.

[0147] In step 446, the thoracic pressure is measured to determinewhether it is within the range from about −15 to about −25 mm Hg. If thenegative intrathoracic pressure is outside of this range, the stimulatoroutput is adjusted as illustrated in step 454 and the process proceedsback to step 432. As previously described, system 400 may be used innon-CPR applications as well. In such situations, step 446 may beemployed to ensure that the negative intrathoracic pressure within thepatient remains within a desired range.

[0148] If the automatic mode is selected, the process proceeds to step448 where the rescuer has the option of setting the stimulation rate,preferably in terms of stimulations per minute. System 400 is thenconfigured to automatically stimulate the phrenic nerve using theelectrodes. System 400 is further configured to produce the electricalsignal with an appropriate pulse train duration and width as shown instep 450. To assist the user in performing chest compressions in asynchronized manner with diaphragmatic stimulation, the process includesstep 452 where an appropriate audio-visual signal is produced toindicate to the rescuer when chest compressions should be performed. Inanother embodiment, the stimulator is turned on to stimulate the phrenicnerve at a given rate and the rescuer times the delivery of chestcompressions based upon when the phrenic nerve is stimulated. Chestcompressions are then delivered after each stimulation.

EXAMPLES

[0149] Various electrode mapping and electroventilation studies wereperformed to illustrate exemplary electrode placement strategies. Thestudies also focused on the type of electrical wave form and othercharacteristics of the stimulating signal, as well as the use of aninspiratory threshold valve to control the flow of respiratory gases tothe lungs. It will be appreciated that the following examples are merelyillustrative of certain electrode configurations, and that the inventionis not intended to be limited only to the specific examples shownhereinafter.

[0150] The following examples evaluate the required energy to produce agiven negative intrathoracic pressure. The examples were performed in28-33 Kg female domestic pigs. A Grass S44 (Astro-Med, Inc.) square wavestimulator was modified to deliver either a monophasic or asymmetricalbiphasic wave form at zero to 450 mA.

Example 1:

[0151] In this example, gel electrodes, having an outer dimension of 5cm by 5 cm, were placed as shown in FIG. 23. An electrode control box(not shown) was developed to control the current flow between anyelectrode pair combinations. The electrodes were not removed or replacedduring the study.

[0152] The invention utilized electrode pairs 500, 502, 504, 506 and508. The medial edge of each electrode was placed 8 cm laterally from amidline 510 defined by the sternum 512, and 1 cm apart from each othersuperior to inferior from the xiphoid line 514. In an attempt todecrease the negative intrathoracic pressure during a stimulatory pulsestream, an impedance threshold valve was used to occlude the airwayuntil a negative intrathoracic pressure of −22 cm H₂O was reached. Atthis pressure, the valve was permitted to open, thereby allowinginspiratory air flow. The impedance threshold valve was similar to thatdescribed in U.S. Pat. Nos. 5,551,420 and 5,692,498, previouslyincorporated by reference.

[0153] The study was conducted in an anesthetized female domestic pigduring normal profusion and sinus rhythm. Positive pressure ventilationwas set at 12-16 breaths/minute and each stimulation pulse trainoccurred during the exhalation cycle of respiratory gas exchange. Allstudies measured the amount of negative intrathoracic pressure (mm-Hg)for each individual electrode pair or electrode pair combination. At 25Hz, 110 volts, 250 microseconds pulse width, a 750 millisecond to 1second monophasic pulse train was delivered during the exhalation cycle.The mean negative intrathoracic pressure values for each electrode pairare shown in Table 1. TABLE 1 Electrode Pair Mean-ITP (mmHg) 500 8.75502 8.02 504 6.62 506 2.50 508 1.16

[0154] The data in Table 1 indicates that as transthoracic current isdelivered to stimulate each hemisphere of the diaphragm, the electrodepair closest to the xiphoid line and thus superficially closer to thediaphragm, produced the greatest negative intrathoracic pressuredeflection.

Example 2

[0155] The study of Example 2 was set up essentially identical to thatof Example 1 except that the electrodes were stimulated in differentpaired combinations. Electrode pair combinations produced a simulatedelectrode in which the surface area was increased according to thenumber of electrode pair combinations used. In Example 2, the electricalwave form patterns were changed to 30 Hz, 120 volts, 500 microsecondsmonophasic pulse width. The results of this study are shown in Table 2.TABLE 2 Electrode Pair Combination Mean-ITP (mmHg) 500/502 11.25 502/5049.50 504/506 7.01 500/504 10.75 500/502/504 10.77 500/502/504/506 10.37

[0156] The data of Example 2 indicates that as transthoracic current isdelivered between electrode pair combinations, the surface area of thesimulated electrode disbursed the current which enabled a strongercontraction of the diaphragm and thus a greater negative intrathoracicpressure.

Example 3

[0157] The study of Example 3 utilized the 500/502/504 electrode paircombination at 50 Hz to 70 Hz, 90 volts, 500 microsecond monophasicpulse width. Blood gases were taken at the onset of each frequencychange to monitor pH and determine if fatigue was apparent due to theincrease in lactic acid and thus a decrease in pH. The results of thisstudy are shown in Table 3. TABLE 3 Pulse Train Frequency (Hz) Mean-ITP(mmHg) 50 11.30 60 11.78 70 12.50

[0158] The data of Example 3 illustrates that an increase in frequencyhad a slight positive effect on increasing the magnitude of negativeintrathoracic pressure. However, the pH became more acidic. Thisindicates that as the frequency increases, fatigue becomes more apparentand is reflected in a decrease in the magnitude of negativeintrathoracic pressure and a decrease in pH due to lactic acidaccumulation.

Example 4

[0159] In this study, the electrode pair combination 500/502 was used at25 Hz to 70 Hz, 90 volts, 350 microseconds to 500 microsecondsmonophasic pulse width. Blood gases were taken at the onset of eachfrequency change to monitor pH. The results of this study as shown inTable 4. TABLE 4 Pulse Train Frequency Mean-ITP (Hz) Pulse Width (μs)(mmHg) 25 350 7.75 50 350 11.50 25 500 13.00 35 500 20.00 50 500 22.3060 500 20.67 70 500 21.67

[0160] The data of Example 4 indicates that the optimal negativeintrathoracic pressure target of −15 mmHg to −20 mmHg may be achievedduring transthoracic current flow between the 500/502 electrode paircombination. The data also indicates that by lowering the pulse streamfrequency, the acidity of the pH was not as pronounced as in higherfrequency. Moreover, the pulse width of the individual stimulationpulses appears to be optimal at 0 microseconds.

Example 5

[0161] This study utilized the 500/502 transthoracic electrode paircombination to evaluate wider stimulation pulse widths to determine iflarger deflections in negative intrathoracic pressure would occur. Waveform parameters were adjusted at 500 Hz, 80 to 95 volts, 500microseconds to 5000 microseconds monophasic pulse width. Blood gaseswere taken at the onset of each frequency change to monitor pH. Theresults of this study are shown Table 5. TABLE 5 Pulse Width VoltageMean-ITP (μs) (Volts) (mmHg) 500 80 9.33 500 90 20.80 500 95 24.11 100090 23.33 3000 90 22.00 5000 90 20.00

[0162] The results of Example 5 indicate that as pulse width increasedand/or voltage increased, a greater magnitude of negative intrathoracicpressure could be achieved. However, the tradeoff was an increase inacidosis when the pulse width, frequency, or voltage were increased.

[0163] Hence, with examples 1-5, fatigue appeared to be a significantobstacle. Accordingly, one aspect of the invention was to utilize abiphasic wave form to minimize the net charge transfer and thus minimizethe charge accumulation on the electrode/tissue interface. An increasein charge accumulation on the electrode/tissue interfaces decreases netcurrent flow between the stimulating electrodes, thereby reducingcontraction of the diaphragm and reducing the desired deflection innegative intrathoracic pressure.

[0164] Accordingly, the remaining studies focus on stimulating thephrenic nerve in the cervical region of the spine. Anatomically, thephrenic nerve branches from the central nervous system between thecervical spine locations C3 through C5. The phrenic nerve descendsinferior along the external jugular vein into the thoracic cavity. Tostimulate the phrenic nerve in this region, gel electrodes having anouter perimeter of 4 cm by 9 cm were placed as shown in FIG. 24A(anterior locations) and FIG. 24B (posterior locations). As withexamples 1-5, an electrode control box was used to control the currentflow between any electrode pair combination and the electrodes were notremoved or replaced during the study.

[0165] As shown in FIGS. 24A and 24B, ionic current flow was inducedbilaterally anterior to posterior in the cervical region of the spine toinitiate an action potential in the phrenic nerve causing the nerve tobilaterally fire and contract the diaphragm. In FIG. 24A, electrodes areplaced centrally 12 cm from the bony protrusion reference line 518 andcentrally 3 cm laterally from the central line 520. In FIG. 24B, thesuperior electrode is placed 3 cm from reference line 520 that is drawnbetween the bony indentation just behind the ears. The remainingelectrodes are placed 1 cm apart descending in the inferior direction.Simulator electrodes were therefore created with 2 anterior electrodesand 3 posterior electrodes thus creating an anterior to posteriorbipolar electrode configuration.

Example 6

[0166] With such a configuration, studies were conducted withanesthetized female domestic pigs under normal profusion and positivepressure ventilation. An asymmetrical biphasic wave form at a 500microseconds pulse width and a 30 Hz pulse train frequency were fixed.The varying voltage parameter was adjusted between 60 and 150 voltspulsating direct current. The graphs of FIGS. 25-27 displayed the meanresults of the studies.

[0167] The graph of FIG. 25 displays the results of an inspiratorythreshold valve assessment to determine the applicable voltage to obtainthe target negative intrathoracic pressure between −15 mmHg and −20mmHg. As with the previous studies, stimulation occurred during theexhalation cycle of positive pressure ventilation under normalprofusion. As shown, less energy is required to achieve the targetnegative intrathoracic pressure utilizing this electrode configurationin conjunction with an asymmetrical biphasic form compared with otherelectrode configurations as in FIG. 23. Transthoracic electrodeconfigurations required at least 90 volts pulsating DC compared to 60 to70 volts pulsating DC with the cervical electrode configurations toproduce the same deflection in negative intrathoracic pressure.Reproducibility with the cervical electrode configurations has beenachieved in every study without failure.

[0168] The graph of FIG. 26 illustrates the effects of cervical phrenicnerve stimulation and expiratory title volume. The graph of FIG. 26depicts a representation of the amount of voltage required to producethe target negative intrathoracic pressure without the use of animpedance threshold valve. As shown, the amount of energy nearly doublesindicating that more energy is required to decrease the intrathoracicpressure negative without utilizing the impedance threshold valve.

[0169] The graph of FIG. 27 illustrates expiratory title volumesachieved at the corresponding negative intrathoracic pressure. As shown,cervical stimulation of the phrenic nerve generates sufficient gasexchange to sustain life by electroventilation.

[0170] The results of this study indicate that cervical electrodepositioning utilized to initiate an action potential in the phrenicnerve are significantly easier to achieve when compared to transthoracicelectrode configurations. Moreover, electroventilation has been easilyreproduced with cervical phrenic stimulation.

[0171]FIGS. 28A and 28B illustrate another embodiment for singleelectrode placement. This electrode placement is similar to that ofFIGS. 24A and 24B except that single electrodes are used for anteriorand posterior placement.

[0172]FIG. 29 illustrates an embodiment of a stimulation device 500 thatis constructed of a support body 502 comprising a back plate 504 and aneck support 506. Support body 502 may be constructed of essentially anytype of rigid material, such as plastics, acrylics, and the like. Inuse, a patient is placed onto support body 502 such that the patient'sback rests upon back plate 504. Further, neck support 506 is positionedagainst the patient's neck, forcing the patient's head backward to openthe patient's airway. Conveniently, back plate 504 also provides supportto the patient's back when performing CPR.

[0173] Coupled to support body 502 are a pair of electrodes 508 and 510that may be used to electrically stimulate the phrenic nerve in a mannersimilar to that described with previous embodiments. Also coupled tosupport body 502 are a pair of electrodes 512 and 514 that may be usedto provide a defibrillating shock. Ab electrical conductor 516 isprovided to permit device 500 to be coupled to a defibrillator/stimulator to provide electrical current to the various electrodes.Optionally, an electrical port 518 may be provided to hold one or moreelectrical circuits that are to be used in controlling the variouselectrical shocks and/or stimulations supplied by the electrodes.

[0174]FIG. 30 illustrates an alternative embodiment of a stimulationdevice 520 that is constructed of a support body 522 comprising a backplate 524 and a neck support 526 in a manner similar to device 500.Device 520 includes a pair of electrodes 528 and 530. Electrode 528 ispositioned so as to be adjacent the back of the patient's neck, whileelectrode 530 may be placed at the front of the patient's neck tostimulate the phrenic nerve. Although not shown, device 520 may includean electrical conductor to permit device 520 to be coupled to astimulation unit.

[0175] As previously described in connection with FIG. 8A, a neck collarmay be employed to stimulate the phrenic nerve. One embodiment of a neckcollar system 550 is illustrated in FIGS. 31-33. System 550 comprises aneck collar 552 having two ends 554 and 556 that may be separated fromeach other to permit placement of collar 552 about the neck of a patientas shown in FIG. 31. Conveniently, one or more strips 558 of a hook andloop fastener material, such as Velcro fastener material, may be coupledto collar 552 to secure ends 554 and 556 adjacent each other aftercollar 552 has been placed about the neck. However, it will beappreciated that other types of connectors may be used.

[0176] Coupled to collar 552 by elastic straps 560 and 562 is a facemask 564 that may include an impedance threshold valve system 566 thatis configured similar to other embodiments described herein. To couplemask 564 to the patient's face, straps 560 and 562 are positioned on topof the patient's head and extend downward to the patient's neck as shownin FIG. 31. Once straps 560 and 562 are positioned, collar 552 ispositioned around the patient's neck and secured into position.

[0177] Once collar 552 is secured in place, collar 552 may be inflatedusing an inflation port 567 to maintain adequate contact between thestimulation electrodes and the surface of the patient's skin. Face mask564 may also be adjusted to the proper position by the use of anadjustable head buckle 568 and the use of fasteners 570 and 572 thatpermit straps 560 and 562, respectively, to slide relative to collar552.

[0178] Disposed within collar 552 are stimulating electrodes 574 tostimulate the phrenic nerve to contract. Electrodes 574 are placed onboth a posterior side 576 and an anterior side 578 to facilitate phrenicnerve stimulation in a manner similar to that described in connectionwith other embodiments. An electrode connector 580 is provided to permitelectrodes 574 to be coupled to a stimulation unit.

[0179]FIG. 34 illustrates another embodiment of a neck collar 590 thatmay be used to stabilize the neck and open the patient's airway. Collar590 further includes stimulation electrodes 590 and 592 for stimulatingthe phrenic nerve in a manner similar to that described in connectionwith other embodiments. Leads 594 are coupled to electrodes 590 and 592to permit the electrodes to be coupled to a stimulation unit.Conveniently, collar 590 may be constructed in two halves to permit eachattachment and removal. Attachment straps 596 may be used to hold thetwo halves together. As previously described, the techniques of theinvention may find use in treating hypovolemic or hemorrhagic shock.Trauma induced hypovolemic shock can be a principal cause of death inhumans. Unfortunately, the chances for survival after trauma andsubsequent blood volume loss are not favorable in environments whererapid rescue attempts and blood volume replenishment are not immediatelyavailable. To aid in improving survival after excessive blood volumeloss and prior to blood volume replenishment, the invention providestechniques and equipment to sustain adequate hemodynamic parameters fora prolonged period of time until volume replenishment can occur.

[0180] Such techniques may employ the use of two components: a system toregulate airflow to the patient's lungs, and a lifting device toactively lift the patient's chest. For example, the invention mayutilize an impedance threshold valve, as described generally in thepreceding text and in U.S. Pat. No. 5,692,498, previously incorporatedby reference. Further, to lift the chest, the invention may utilize anactive chest compression/decompression device, such as those that arecommercially available from Ambu International and described generallyin U.S. Pat. No. 5,645,552, incorporated herein by reference.Alternatively, the invention may utilize any device capable of liftingthe chest including, for example, suction cups, adhesives, and the like.Further such devices may be hand held, manually operated, or automated(such as a piston having a suction cup at a bottom end). Further, aspreviously described, phrenic nerve stimulation may be used to decreasethoracic pressures. This may be used alone or in combination with activelifting of the chest.

[0181] During hypovolemic shock, systolic blood pressures can often dropto extremely low levels resulting in minimal blood perfusion and tissueischemia. To improve hemodynamics during hypovolemic and other types ofshock, one method controls incoming airflow and actively lifts the chestto decrease intrathoracic pressure and increase venous return to theright chambers of the heart from the peripheral venous vasculature. Forexample, the sternum and the anterior rib cage may be actively lifted.The increased venous blood volume return thus increases cardiac chamberfilling volumes and greatly improves hemodynamic parameters in patientswith a functional beating heart.

[0182] In one specific embodiment, the method utilizes a suction cupdevice 600 as shown in FIGS. 35 and 36 that attaches to the patient'schest. The suction cup device 600 creates a vacuum seal with thepatient's chest allowing the rescuer to lift up on a handle 602 andraise the patient's thoracic cavity. Raising the thoracic cavity lowersthe intrathoracic pressure and increases venous return from theperipheral vasculature to the beating heart. Repeatedly raising andlowering the patient's thoracic cavity creates a vacuum pumpingmechanism that enhances central venous return and improves overallcardiopulmonary circulation. In cases where the patient is essentiallylacking a blood pressure, the patient's chest may be actively liftedwithout also compressing the chest. However, if the patient has amoderate blood pressure, the patient's chest may optionally becompressed in an alternating manner with chest decompressions.

[0183] The volume of venous return is further enhanced by lowering theintrathoracic pressure more negatively with the use of an impedancethreshold valve. The impedance threshold valve functions to increasecentral venous return by impeding airflow into a patient's lungs duringchest elevation, thus enhancing the extent and duration of negativeintrathoracic pressure. The impedance threshold valve is connected tothe patient's airway through use of an external face mask, an internalendotracheal tube inserted into the patient's trachea during intubation,or the like. Merely by way of example, when treating hemorrhagic shock,the patient's chest may be actively lifted in the range from about 20 toabout 60 times per minute. Further, the impedance valve may be set toprevent air flow to the lungs until reaching a negative intrathoracicpressure that is in the range from about −5 to about −30 cmH₂O.Periodically, the patient may also be ventilated.

[0184] The enhanced extent and duration of negative intrathoracicpressure during chest elevation and the impedance of inspiratory airflowpromotes venous blood flow into the heart and lungs from the peripheralvenous vasculature. Increased venous return aids the beating heart incirculating more oxygenated blood to the vital organs under hypovolemicshock conditions. Therefore, the increase in systemic circulatory flowand systolic blood pressure produced by this method significantlyreduces ischemia in vital organ or peripheral tissue vasculature. Theincrease in tissue perfusion can be sustained for a prolonged period oftime utilizing this method and devices prior to volume replenishment andfurther rescue attempts.

[0185] The invention has now been described in detail. However, it willbe appreciated that certain changes and modifications may be made.Therefore, the scope and content of this invention are not limited bythe foregoing description. Rather, the scope and content are to bedefined by the following claims.

What is claimed is:
 1. A method for increasing blood flow to the thoraxof a patient, the method comprising: periodically stimulating thephrenic nerve to cause the diaphragm to contract and thereby cause anincrease in the magnitude and duration of negative intrathoracicpressure; and periodically occluding airflow to the lungs duringcontraction of the diaphragm with a valve that is positioned to controlairflow into the patient's airway to further increase the magnitude andduration of negative intrathoracic pressure, thereby forcing more bloodinto the thorax.
 2. A method as in claim 1, wherein the stimulating stepcomprises applying electrical current to the phrenic nerve withelectrode that are positioned over the cervical vertebrae between C3 andC7.
 3. A method as in claim 2, wherein the stimulating step furthercomprises placing the electrodes both posterior and anterior between C3and C5.
 4. A method as in claim 2, wherein the electrical current isprovided in monophasic or multiphasic form.
 5. A method as in claim 4,wherein the multi-phasic form comprises an asymmetrical biphasicwaveform.
 6. A method as in claim 5, wherein the biphasic electricalcurrent is in the range from about 100 milliamps to about 2,000milliamps at a frequency in the range from about 10 Hz to about 100 Hz,and wherein the electrical current is supplied in pulse widths in therange from about 1 μs to about 5 ms.
 7. A method as in claim 1, whereinthe patient is suffering from hemorrhagic shock, and wherein thestimulating step further comprises stimulating the phrenic nerve about 5to about 30 times per minute.
 8. A method as in claim 7, wherein thephrenic nerve is stimulated after each breath for time intervals ofabout 0.25 seconds to about 5 seconds.
 9. A method as in claim 7,wherein the phrenic nerve is stimulated to contract in the range fromabout twice per every one breath to about once about every five breaths.10. A method as in claim 1, wherein the patient is suffering fromhypovolemic shock, and wherein the stimulating step further comprisesstimulating the phrenic nerve about 3 to about 30 times per minute. 11.A method as in claim 1, wherein the patient is suffering fromcardiogenic shock, and wherein the stimulating step further comprisesstimulating the phrenic nerve about 5 to about 80 times per minute. 12.A method as in claim 1, wherein the patient is suffering from cardiacarrest, wherein the stimulating step further comprises stimulating thephrenic nerve about 10 to about 80 times per minute, and furthercomprising repeatedly compressing the chest at a rate in the range fromabout 60 compressions to about 100 compressions per minute.
 13. A methodas in claim 12, further comprising sensing the chest compressions andstimulating the phrenic nerve based on the sensed compressions.
 14. Amethod as in claim 12, further comprising indicating to a rescuer whento perform the chest compressions based on the timing of phrenic nervestimulation.
 15. A method as in claim 12, further comprising countingthe number of chest compressions relative to the number of phrenic nervestimulations.
 16. A method as in claim 1, wherein the patient issuffering from post resuscitation pulseless electrical activity, andwherein the stimulating step further comprises stimulating the phrenicnerve about 10 to about 80 times per minute.
 17. A method as in claim 1,wherein the patient is suffering from right ventricular failure, whereinthe stimulating step further comprises stimulating the phrenic nerveabout 5 to about 80 times per minute.
 18. A method as in claim 2,further comprising sensing the magnitude of negative intrathoracicpressure and adjusting the current supplied to the electrodes based onthe measurement so that the magnitude of negative intrathoracic pressureremains within the range from about −5 mmHg to about −30 mmHg afterdiaphragmatic stimulation.
 19. A method for stimulating the phrenicnerve of a patient, the method comprising: placing electrodes posteriorand anterior in the region of the cervical vertebrae; and periodicallyapplying electrical current having a multi-phasic waveform to theelectrodes to stimulate the phrenic nerve, thereby causing the diaphragmto contract.
 20. A method as in claim 19, wherein the multi-phasic waveform comprises an asymmetrical biphasic waveform.
 21. A method as inclaim 20, wherein the biphasic electrical current is in the range fromabout 100 milliamps to about 2,000 milliamps at a frequency in the rangefrom about 10 Hz to about 100 Hz, and wherein the electrical current issupplied in pulse widths in the range from about 1 μs to about 5 ms. 22.A method as in claim 19, wherein the patient is suffering fromrespiratory distress or apnea, and wherein the stimulating stepcomprises stimulating the phrenic nerve about 10 to about 30 times perminute.
 23. A method for ventilating a patient, the method comprising:placing electrodes posterior and anterior in the C3 to C5 region of thecervical vertebrae; and periodically applying electrical current havinga monophasic or biphasic waveform to the electrodes to stimulate thephrenic nerve, thereby causing the diaphragm to contract and drawrespiratory gases into the patient's lungs.
 24. A method as in claim 23,wherein the stimulating step comprises stimulating the phrenic nerveabout 10 to about 30 times per minute.
 25. A method for increasing bloodflow to the thorax of a patient, the method comprising: repeatedlyelectrically stimulating the diaphragm to contract with at least twoelectrodes; sensing the magnitude of negative intrathoracic pressureafter diaphragmatic stimulation; and controlling the amount of currentsupplied to the electrodes based on the measured pressure.
 26. A methodas in claim 25, further comprising controlling the amount of current sothat the magnitude of negative intrathoracic pressure is within therange from about −5 mmHg to about −30 mmHg after diaphragmaticstimulation.
 27. A method as in claim 25, further comprising stimulatingthe phrenic nerve in the region of the cervical vertebrae to stimulatediaphragmatic contraction.
 28. A method as in claim 27, wherein theelectrodes are placed posterior and anterior in the C3 to C5 region ofthe cervical vertebrae, and further comprising applying electricalcurrent having an asymmetric biphasic waveform to the electrodes tostimulate the phrenic nerve.
 29. A medical kit for increasing blood flowto the thorax, the method comprising: at least one electrode that isadapted to be placed over the cervical vertebrae to stimulate thephrenic nerve when actuated; a controller to which the electrode iselectrically coupled, wherein the controller is configured to supplyelectrical current to the electrode to electrically stimulate thephrenic nerve, thereby causing the diaphragm to contract; a valve thatis configured to prevent the flow of respiratory gases into the lungsuntil a certain negative intrathoracic pressure is exceeded, at whichtime the valve opens to permit the flow of respiratory gases into thelungs.
 30. A medical kit as in claim 29, further comprising a pair ofelectrodes that are adapted to be placed posterior and anterior in theC3 to C6 region of the cervical vertebrae.
 31. A medical kit as in claim30, wherein the controller is configured to produce biphasic electricalcurrent that is in the range from about 100 milliamps to about 2,000milliamps at a frequency in the range from about 10 Hz to about 100 Hz,and wherein the controller is configured to supply the electricalcurrent in pulse widths in the range from about 1 μs to about 5 ms. 32.A system for increasing blood flow to the thorax, the system comprising:a collar that is configured to be placed around the neck in a securedarrangement; and at least two electrodes coupled to the collar such thatthe electrodes are positioned posterior and anterior to cervicalvertebrae C3 to C6 when the collar is secured about the neck.
 33. Asystem as in claim 32, further comprising a controller that isconfigured to supply electrical current to the electrodes to stimulatethe phrenic nerve.
 34. A method for increasing blood flow to the thorax,the method comprising: placing a collar having at least two electrodesaround a patient's neck in a secured arrangement such that the twoelectrodes are positioned posterior and anterior to the cervicalvertebrae C3 to C6; and periodically supplying electrical current to theelectrodes to stimulate the phrenic nerve to cause the diaphragm tocontract and thereby cause an increase in the magnitude and duration ofnegative intrathoracic pressure to force more blood into the thorax. 35.A method as in claim 34, further comprising periodically occludingairflow to the lungs during contraction of the diaphragm with a valvethat is positioned to control airflow into the patient's airway tofurther increase the magnitude and duration of negative intrathoracicpressure, thereby forcing more blood into the thorax.
 36. A stimulationdevice, comprising: a generally flat back plate that is configured to beplaced below a patient's back when the patient is lying down; a necksupport that is coupled to the back plate, wherein the neck support israised relative to the back plate and is adapted to tilt the patient'shead backward; and at least two electrodes coupled to the stimulationdevice that are adapted to electrically stimulate the patient.
 37. Adevice as in claim 36, wherein the electrodes comprise phrenic nervestimulation electrodes.
 38. A device as in claim 37, further comprisinga pair of defibrillation electrodes coupled to the stimulation device.39. A method for increasing blood flow to the thorax of a patientsuffering from hemorrhagic shock, the method comprising: periodicallylifting the patient's chest to cause an increase in the magnitude andduration of negative intrathoracic pressure; and periodically occludingairflow to the lungs during contraction of the diaphragm with a valvethat is positioned to control airflow into the patient's airway tofurther increase the magnitude and duration of negative intrathoracicpressure, thereby forcing more blood into the thorax.
 40. A method as inclaim 39, further comprising lifting the chest about 20 to about 60times per minute, and occluding airflow until the negative intrathoracicpressure exceeds a pressure in the range from about −5 to about −30cmH₂O.
 41. A method as in claim 39, further comprising lifting the chestwith a suction cup device and occluding airflow with an impedancethreshold valve.